The hyperpolarization-activated cyclic-nucleotide-gated
non-selective cation (HCN) channels play a potential role in the
neurological basis underlying drug addiction. However, little is
known about the role of HCN channels in methamphetamine
(METH) abuse. In the present study, we examined the changes
in working memory functions of METH re-exposed mice through
Morris water maze test, and investigated the protein expression
of HCN1 channels and potential mechanisms underlying the
modulation of HCN channels by Western blotting analysis. Mice
were injected with METH (1 mg/kg, i.p.) once per day for
6 consecutive days. After 5 days without METH, mice were
re-exposed to METH at the same concentration. We found that
METH re-exposure caused an enhancement of working memory,
and a decrease in the HCN1 channels protein expression in both
hippocampus and prefrontal cortex. The phosphorylated
extracellular regulated protein kinase 1/2 (p-ERK1/2),
an important regulator of HCN channels, was also obviously
reduced in hippocampus and prefrontal cortex of mice with METH
re-exposure. Meanwhile, acute METH exposure did not affect the
working memory function and the protein expressions of HCN1
channels and p-ERK1/2. Overall, our data firstly showed the
aberrant protein expression of HCN1 channels in METH
re-exposed mice with enhanced working memory, which was
probably related to the down-regulation of p-ERK1/2 protein
expression.
MK-801 impaired social recognition potency of adult male rats when given immediately after the initial interaction with a juvenile rat. Administration of kynurenic acid prior to the initial interaction protected the adults against recognition deficits induced by MK-801. When re-exposed at a delay of 30 min to the familiar juvenile, social investigation in the adults was significantly reduced. Thus, the adults are able to remember olfactory stimuli emitted by juvenile con-specifics., Z. Hliňák, I. Krejčí., and Obsahuje bibliografii